Prostaglandins & other lipid mediators最新文献

Introduction

Methods

Results

Conclusions

Aim

Methods

Results

Conclusion

Introduction

Dyslipidemia with a considerable progression rate is a primary risk factor for CVDs if left untreated. Dietary interventions have explored the health influences of selenium on lipid profiles in adults, yet the findings remain contentious. This study seeks to determine if selenium supplementation can positively modify the lipid profile (total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), very-low-density lipoprotein cholesterol (VLDL), and high-density lipoprotein cholesterol (HDL-C) in adults.

Methods

Using predefined keywords, we searched online databases, including Scopus, PubMed, Web of Science Core Collection, and Google Scholar, for relevant studies published from inception through July 2024. A random-effects meta-analysis was then employed to pool the weighted mean differences (WMD) and 95 % CI for outcomes assessed by a minimum of three studies.

Results

Initially 1205 studies were obtained out of which 25 RCTs were decided to be included for further analyses. Selenium supplementation reduced VLDL (WMD: −1.53; 95 % CI: −2.86, −0.20), but did not change TG (WMD: 1.12; 95 % CI: −4.51, 6.74), TC (WMD: −2.25; 95 % CI: −6.80, 2.29), LDL-C (WMD: 1.60; 95 % CI: −4.26, 7.46), and HDL-C levels (WMD: 0.98; 95 % CI: - 0.02, 1.98).

Conclusion

Our study showed significantly reduced VLDL but limited effects were observed in other lipid indexes. More extensive RCTs are required globally to achieve a holistic comprehension of the connection between selenium and lipid profile.

Transient receptor potential melastatin 7 (TRPM7) has been emerged as a potent drug target for immunomodulation with ion conductance and kinase activities. The research is projected to characterize the influences of TRPM7 on the course of ulcerative colitis (UC) and dissect the latent response mechanisms. The in vivo murine model and in vitro cell model of UC were both stimulated by DSS. RT-qPCR and western blotting tested the abundance of TRPM7. Colonic damage was estimated by Hematoxylin-eosin staining, calculation of colon length, measurement of DAI and MPO assay kit. CCK-8 method and TUNEL staining severally ascertained cell activity and apoptosis. ELISA method assayed the inflammatory levels and relevant assay kits determined oxidative stress levels. FITC-dextran flux, immunohistochemistry, TEER as well as western blotting evaluated intestinal barrier function. Immunofluorescence staining and western blotting appraised NLR family pyrin domain containing 3 (NLRP3)-dependent pyroptosis. Depleted TRPM7 retarded inflammation, oxidative damage as well as intestinal barrier damage both in vitro and in vivo. TRPM7 reduction repressed the pyroptosis mediated by NLRP3 inflammasome. NLRP3 agonist nigericin partly abolished the protection elicited by TRPM7 silencing against inflammation, oxidative damage as well as intestinal barrier damage in vitro. Collectively, TRPM7 deletion might possess the therapeutic potential in UC, the working mechanism of which might involve the inactivation of NLRP3-dependent pyroptosis.

Hyperlipidemia, obesity and gut dysbiosis are pivotal risk factors for atherosclerotic cardiovascular disease (ACVD). Supplementation of Akkermansia muciniphila (AKK) has also been proven to be effective in the prevention and treatment of obesity and other metabolic disorders. Here we found that AKK was more abundant in healthy control than ACVD patients via metagenomic sequencing on fecal samples. Subsequently, we investigated the role and underlying mechanism of AKK on obesity-associated atherosclerosis. AKK intervention partially reversed the exacerbation of atherosclerotic lesion formation in ApoE^-/- mice by improving dyslipidemia. Interestingly, replenishment with AKK significantly enhanced cardiac function and reduced the body weight. It also reduced pro-inflammatory cytokine IL-6 and increased anti-inflammatory IL-10 in the circulation. Additionally, AKK colonization dramatically regulated gut microbiota and increased the abundance of Lactobacillaceae. Our findings have provided novel insights into the therapeutic potential of AKK as a beneficial microbe for treating atherosclerotic-associated cardiovascular diseases.

Curcumin, an inherent polyphenolic compound, has the potential to influence glycemic indices. Nevertheless, the conclusions drawn from extant meta-analyses remain contentious. To determine the impact of curcumin supplementation on these indices, the current umbrella meta-analysis included existing systematic reviews and meta-analyses. A thorough systematic search was conducted using databases Embase, PubMed, WOS, Scopus, and the Cochrane Library to acquire peer-reviewed literature published before January 2024. The random-effects model was employed to conduct a meta-analysis. The present analysis incorporated a total of 22 meta-analytic studies. The findings of our study indicate that the administration of curcumin supplements leads to a significant decrease in fasting blood sugar levels (FBS) (ES: −1.63; 95 % CI: −2.36, −0.89, P<0.001; I²=88.4 %, P<0.001), homeostasis model assessment-estimated insulin resistance (HOMA-IR) (ES: −0.38; 95 % CI: −0.48, −0.28, P<0.001; I²=35.9 %, P=0.142), hemoglobin A1c (HbA1c) (ES: −0.44; 95 % CI: −0.67, −0.21, P<0.001; I²=65.0 %, P=0.014), and insulin (ES: −0.86; 95 % CI: −1.52, −0.21, P=0.010; I²=92.5 %, P<0.001). The results of this study suggest that the administration of curcumin supplements may be a beneficial intervention for enhancing glycemic indices.